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Decoy Peptides: Development of a Novel Therapeutic for Metastatic Cancer

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R41CA173937-01A1
Agency Tracking Number: R41CA173937
Amount: $300,000.00
Phase: Phase I
Program: STTR
Solicitation Topic Code: NCI
Solicitation Number: PA12-089
Timeline
Solicitation Year: 2013
Award Year: 2013
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
5540 E PASEO CIMARRON
TUCSON, AZ 85750-1101
United States
DUNS: 21115879
HUBZone Owned: No
Woman Owned: Yes
Socially and Economically Disadvantaged: No
Principal Investigator
 TODD CAMENISCH
 (520) 955-1948
 camenisch@pharmacy.arizona.edu
Business Contact
 TODD CAMENISCH
Phone: (520) 955-1948
Email: camenisch@pharmacy.arizona.edu
Research Institution
 UNIVERSITY OF ARIZONA
 
UNIVERSITY OF ARIZONA PO BOX 210158, Room 510
TUCSON, AZ 85721-0158
United States

 () -
 Nonprofit College or University
Abstract

DESCRIPTION (provided by applicant): Arizona Cancer Therapeutics LLC (ACT) proposes a two-year, preclinical research project in cooperation with the University of Arizona Cancer Center to develop the novel anti-tumor therapeutic, Protein transduction domain-MUC1 Inhibitory Peptide (PMIP). PMIP is an intracellular MUC1 peptide that acts as a decoy to block the MUC1- oncoprotein interactions that drive breast cancer growth and metastasis. Utilizing a protein transduction domain to allow for transmembrane cellular uptake, PMIP can freely enter the cell and interact with intracellular target proteins. Laboratory research at the University of Arizona over the past nine years has examined the ability of MUC1 and an oncogenic partner, epidermal growth factor receptor (EGFR), to synergistically drive breast cancer progression. To block these tumor-specific, intracellular interactions, the first-in-class peptide-based cancer therapeutic, PMIP, was developed. Studies in tumor-bearing mouse models demonstrate that PMIPblocks tumor growth and metastasis and is nontoxic and tumor specific, making it an excellent anti-tumor drug candidate to carry forward through preclinical studies and clinical trials. Over 40,000 Americans die annually from metastatic breast cancer and,in greater than 90 percent of human breast carcinomas and metastases, MUC1 is over-expressed. This project represents critical steps in preclinical studies in drug dosing, absorption, distribution, metabolism and toxicity. The project will also investigatethe benefits of PMIP when used in combination with FDA-approved chemotherapies for breast cancer. PMIP represents a unique approach to targeting MUC1 activities in cancer - other clinical trials targeting MUC1 have been designed to elicit anti-MUC1 immunity, and have been largely ineffective. Unlike these approaches, PMIP does not rely on activation of the immune response, but instead directly blocks tumor-promoting intracellular interactions. If successful, PMIP can substantially enhance the effective treatment options for metastatic breast cancer patients. This project aligns to NIH's mission to enhance health, lengthen life, and reduce the burdens of illness and disability by researching a new and unique anti-tumor drug to treat, effectively and with low or no toxicity, metastatic breast cancer. PUBLIC HEALTH RELEVANCE PUBLIC HEALTH RELEVANCE: Arizona Cancer Therapeutics, LLC (ACT) proposes a two-year preclinical research project to develop a new anti-tumor drug, Protein transduction domain-MUC1 Inhibitory Peptide (PMIP). PMIP has been shown to block specific interactions inside cancer cells that drive tumor growth in metastatic breast cancer and has a high potential to substantially enhance treatment options for these patents. This project, byresearching a new and unique anti-tumor drug to treat a cancer that results in 40,000 deaths in the U.S. annually, aligns to the National Institute of Health's mission to enhance health, lengthen life, and reduce the burdens of illness and disability.

* Information listed above is at the time of submission. *

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